RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells
Braz. j. med. biol. res
;
47(1): 24-34, 01/2014. graf
Article
Dans Anglais
| LILACS
| ID: lil-697676
ABSTRACT
Fanconi anemia complementation group F protein (FANCF) is a key factor, which maintains the function of FA/BRCA, a DNA damage response pathway. However, the functional role of FANCF in breast cancer has not been elucidated. We performed a specific FANCF-shRNA knockdown of endogenous FANCF in vitro. Cell viability was measured with a CCK-8 assay. DNA damage was assessed with an alkaline comet assay. Apoptosis, cell cycle, and drug accumulation were measured by flow cytometry. The expression levels of protein were determined by Western blot using specific antibodies. Based on these results, we used cell migration and invasion assays to demonstrate a crucial role for FANCF in those processes. FANCF shRNA effectively inhibited expression of FANCF. We found that proliferation of FANCF knockdown breast cancer cells (MCF-7 and MDA-MB-435S) was significantly inhibited, with cell cycle arrest in the S phase, induction of apoptosis, and DNA fragmentation. Inhibition of FANCF also resulted in decreased cell migration and invasion. In addition, FANCF knockdown enhanced sensitivity to doxorubicin in breast cancer cells. These results suggest that FANCF may be a potential target for molecular, therapeutic intervention in breast cancer.
Texte intégral:
Disponible
Indice:
LILAS (Amériques)
Sujet Principal:
Mouvement cellulaire
/
Prolifération cellulaire
/
Protéine du groupe de complémentation F de l'anémie de Fanconi
/
Antinéoplasiques
Limites du sujet:
Humains
langue:
Anglais
Texte intégral:
Braz. j. med. biol. res
Thème du journal:
Biologie
/
Médicament
Année:
2014
Type:
Article
/
descriptif de projet
Pays d'affiliation:
Chine
Institution/Pays d'affiliation:
China Medical University/CN
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